Targeting IL-22 and IL-22R protects against experimental osteoarthritis

Osteoarthritis(OA)is characterized by cartilage degradation,pain,and synovitis.1 Joint inflammation driven by cytokines has been demonstrated to cause cartilage degradation and pain.2 However,approaches to neutralize cytokines,such as IL-1 and TNF-α,known to be involved in OA have shown poor clinical efficacy.3 There is an unmet clinical need to find better anti-inflammatory and pain targets for OA therapy and to elucidate the role of other cytokines in OA pathogenesis.Previous studies have shown that IL-22 and its receptor IL-22R play central roles in inflammation and diseases such as psoriasis,ulcerative colitis,graft-versus-host disease,certain infections and tumors,as well as in liver and pancreas damage.4,5 The role of IL-22/IL-22R and the potential for therapeutic targeting of both proteins in OA remain largely unknown,which we sought to investigate.